Cellular and molecular mechanisms of AKI

Anupam Agarwal, Zheng Dong, Raymond Harris, Patrick Murray, Samir M. Parikh, Mitchell H. Rosner, John A. Kellum, Claudio Ronco

Research output: Contribution to journalReview article

68 Scopus citations

Abstract

In this article, we review the current evidence for the cellular and molecular mechanisms of AKI, focusing on epithelial cell pathobiology and related cell-cell interactions, using ischemic AKI as a model. Highlighted are the clinical relevance of cellular and molecular targets that have been investigated in experimental models of ischemic AKI and how such models might be improved to optimize translation into successful clinical trials. In particular, development of more context-specific animal models with greater relevance to human AKI is urgently needed. Comorbidities that could alter patient susceptibility to AKI, such as underlying diabetes, aging, obesity, cancer, and CKD, should also be considered in developing these models. Finally, harmonization between academia and industry for more clinically relevant preclinical testing of potential therapeutic targets and better translational clinical trial design is also needed to achieve the goal of developing effective interventions for AKI.

Original languageEnglish (US)
Pages (from-to)1288-1299
Number of pages12
JournalJournal of the American Society of Nephrology
Volume27
Issue number5
DOIs
StatePublished - May 2016

ASJC Scopus subject areas

  • Nephrology

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    Agarwal, A., Dong, Z., Harris, R., Murray, P., Parikh, S. M., Rosner, M. H., Kellum, J. A., & Ronco, C. (2016). Cellular and molecular mechanisms of AKI. Journal of the American Society of Nephrology, 27(5), 1288-1299. https://doi.org/10.1681/ASN.2015070740